title: [Modulation of lung oxidant/antioxidant status by ischemic post-conditioning during ischemia/ reperfusion injury: experiment with rats].
abstract: OBJECTIVE
  To investigate the effects of ischemic post-conditioning (IPO) on the lung endogenous oxidant-antioxidant system and nitric oxide level during the early stage of ischemia/reperfusion (I/R) injury.
  
  
  METHODS
  Twenty four male Sprague-Dawley rats were randomly divided into 3 equal groups: sham-operation (S) group, I/R Group, undergoing ischemia by blocking the lung hilus for 1 h and then reperfusion for 30 min, IPO Group, undergoing blocking the lung hilus for 1 h and then 3 cycles of 10 s ischemia and 10 s reperfusion. Then the rats were killed with their lungs taken out. The levels of glutathione (GSH), nitric oxide (NO), malondialdehyde (MDA), xanthine oxidase (XO), and endogenous antioxidant enzymes, i. e, superoxide dismutase (SOD), and catalase (CAT), and activities of gultathionine peroxidase (GPX) and myeloperoxidase (MPO), a neutrophil accumulation marker, were measured respectively.
  
  
  RESULTS
  In IPO group, Compared with I/R group, antioxidant systems such as the levels of SOD, CAT, GPX, and GSH of IPO Group were (41.4 +/- 4.4 ) U/mg, (19.5 +/- 1.6) U/mg, (168 +/- 13) U/mg, and (1.72 +/- 0.26) U/g, all significantly higher than those of I/R Group [(19.6 +/- 2.8) U/mg, (8.4 +/- 0.8) U/mg, (72 +/- 8) U/mg, and (0.89 +/-+/- 0.07) mg/g respectively, all P < 0.05); and the levels of XO, MPO, and MDA of Group IPO were (50 +/- 6) U/g, (5.0 +/- 0.5) U/g, and (0.91 +/- 0.08) nmol/mg respectively, all significantly lower than those of I/R Group [(83 +/- 8) U/g, (7.6 +/- 0.7) U/g and (1.58 +/- 0.17) nmol/mg respectively, all P < 0.05). The endogenous NO level of IPO Group was (93 +/- 7) micromol/g, significantly higher than that of I/R Group [(22 +/- 4) micromol/g, P < 0.01].
  
  
  CONCLUSIONS
  Post-conditioning at onset of reperfusion reduces lung I/R injury. The lung protection of IPO may be mediated, in part, by inhibiting the oxidant generation and oxidizing, and may be associated with the increasing of the endogenous NO level.
authors.affiliation: Department of Thoracic and Cardiovascular Surgery, Second Affiliated Hospital of Shantou University Medical College, Shantou 515041, China.
authors.forename: Xu-Guang
authors.initials: XG
authors.lastname: Rao
authors.forename: Li-Min
authors.initials: LM
authors.lastname: Ma
authors.forename: Ming-Ke
authors.initials: MK
authors.lastname: Duan
authors.forename: Tao
authors.initials: T
authors.lastname: Wang
authors.forename: Bo-Liang
authors.initials: BL
authors.lastname: Chen
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D004195:Disease Models, Animal; D007511:Ischemia / Q000503:physiopathology*; D008168:Lung / Q000098:blood supply / Q000378:metabolism*; D008171:Lung Diseases / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D016877:Oxidants / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000503:physiopathology*; D013482:Superoxide Dismutase / Q000378:metabolism; D013997:Time Factors
chemical_list: D000975:Antioxidants; D016877:Oxidants; D009569:Nitric Oxide; D008315:Malondialdehyde; D013482:Superoxide Dismutase